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BACKGROUND: Benzo(a)pyrene (B[a]P) is the most widely concerned polycyclic aromatic hydrocarbons (PAHs), which metabolizes benzo(a)pyrene-7,8-dihydrodiol-9,10-epoxide (BPDE) in vivo to produce carcinogenic effect on the body. Currently, there is limited research on the role of the variation of metabolic enzymes in this process. METHODS: We carried out a study including 752 participants, measured the concentrations of 16 kinds PAHs in both particle and gaseous phases, urinary PAHs metabolites, leukocyte BPDE-DNA adduct and serum BPDE- Albumin (BPDE-Alb) adduct, and calculated daily intake dose (DID) to assess the cumulative exposure of PAHs. We conducted single nucleotide polymorphism sites (SNPs) of metabolic enzymes, explored the exposure-response relationship between the levels of exposure and BPDE adducts using multiple linear regression models. RESULT: Our results indicated that an interquartile range (IQR) increase in B[a]P, PAHs, BaPeq, 1-hydroxypyrene (1-OHP), 1-hydroxynaphthalene (1-OHNap) and 2-hydroxynaphthalene (2-OHNap) were associated with 26.53 %, 24.24 %, 28.15 %, 39.15 %, 12.85 % and 14.09 % increase in leukocyte BPDE-DNA adduct (all P < 0.05). However, there was no significant correlation between exposure with serum BPDE-Alb adduct (P > 0.05). Besides, we also found the polymorphism of CYP1A1(Gly45Asp), CYP2C9 (Ile359Leu), and UGT1A1(downstream) may affect BPDE adducts level. CONCLUSION: Our results indicated that leukocyte BPDE-DNA adduct could better reflect the exposure to PAHs. Furthermore, the polymorphism of CYP1A1, CYP2C9 and UGT1A1affected the content of BPDE adducts.

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Tendinopathy is one of the most prevalent sports injury diseases in orthopedics. However, there is no effective treatment or medicine. Recently, the discovery of tendon stem cells (TSCs) provides a new perspective to find new therapeutic methods for Tendinopathy. Studies have shown that oxidative stress will inevitably cause TSCs injury during tendinopathy, but the mechanism has not been fully elucidated. Here, we report the oxidative damage of TSCs induced by H2O2 via ferroptosis, as well, treatment with H2O2 raised the proportion of mitochondria engulfed by autophagosomes in TSCs. The suppression of mitophagy by Mdivi-1 significantly attenuates the H2O2-induced ferroptosis in TSCs. Mechanically, H2O2 actives the cGAS-STING pathway, which can regulate the level of mitophagy. Interfering with cGAS could impair mitophagy and the classical ferroptotic events. In the rat model of tendinopathy, interference of cGAS could relieve tendon injury by inhibiting ferroptosis. Overall, these results provided novel implications to reveal the molecular mechanism of tendinopathy, by which pointed to cGAS as a potential therapeutic target for the treatment of tendinopathy.

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Li-ion batteries are expected to become the mainstream devices for green energy storage or power supply in the future due to their advantages of high energy and power density and long cycle life. Monitoring the temperature and strain change characteristics of Li-ion batteries during operation is conducive to judging their safety performance. The hinged differential lever sensitization structure was used for strain sensitization in the design of an FBG sensor, which also allowed the simultaneous measurement of strain and temperature. The temperature and strain variation characteristics on the surface of a Li-ion soft-packed battery were measured using the des.igned sensor. This report found that the charging and discharging processes of Li-ion batteries are both exothermic processes, and exothermic heat release is greater when discharging than when charging. The strain on the surface of Li-ion batteries depends on electrochemical changes and thermal expansion effects during the charge and discharge processes. The charging process showed an increasing strain, and the discharging process showed a decreasing strain. Thermal expansion was found to be the primary cause of strain at high rates.

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One-dimensional carbon-based materials have emerged as promising electromagnetic wave absorption agents due to their outstanding conductivity, high stability, low weight, and easy availability. Properly optimizing their electromagnetic parameters is expected to further enhance the electromagnetic wave attenuation capacity. In this work, efficient Cu9S5/C nanocomposite fibers are prepared by a combined approach of electrospinning and subsequent carbonization-sulfurization processes. The Cu9S5 nanoparticles with size of ca. 100-200 nm were homogeneously embedded in fibrous carbon matrix with diameter of 300 nm. For electromagnetic wave absorption, the optimized composited nanofibers (Cu9S5/C-3) exhibited an extremely superb reflection loss of -65.4 dB (9.5 GHz, 2.7 mm) at a lower mass fraction (20 wt%). And the effective absorption bandwidth could be up to 4.1 GHz (8.0-12.1 GHz) with a matching thickness of 2.9 mm, covering the whole X-band. Electromagnetic wave attenuation mechanism investigation revealed that the performance enhancement originated from the synergy of various loss pathways, including interfacial polarization, dipole polarization, and conductive loss. The unique hierarchical structure from particle embedding, one-dimensional fiber, to three-dimensional network further amplified the performance advantages of each component. This work is anticipated to provide a feasible strategy to synthesize sulfide/carbon binary composite fibers for efficient electromagnetic wave absorption.

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The development of a highly efficient and stable catalyst for preferential oxidation of CO for the commercialization of proton-exchange membrane fuel cells has been a result of continuous effort. The main challenge is the simultaneous control of abundant active sites and interfacial reducibility over the catalyst CuxO/CeO2. Here, we report a strategy to modulate porosity, active sites, and O-vacancy sites (OV) by reducing media and O2/H2 activation. O2-pretreated CeO2-supported Cu catalysts unequivocally demonstrate the low-temperature activity owing to the excess concentrations of Cu+ and Cu2+ as well as the relative population of Ce3+ and O-vacancy sites at the surface. O2 activation improves the Cu2+ diffusion into the CeO2 lattice to generate the synergistic effect and induces the formation of electron-enriched Cu2+-OV-Ce3+ sites, which accelerate the activation and dissociation of CO/O2 and the formation of reactive oxygen species during catalysis. Density function theory (DFT) calculations reveal that CO adsorbs on Cu2O {110} and CuO {111} with relatively optimal adsorption energy and longer C-Cu lengths in contrast to that on Cu {111}, favoring the adsorption and desorption of CO. These are crucial for ongoing CO oxidation, producing CO2 by the Mars-van Krevelen mechanism.

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Polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans (PCDD/Fs), and dioxin-like polychlorinated biphenyls (dl-PCBs) are bioaccumulative compounds that may affect fetal growth and infant development. The aim of this study was to determine whether the pregnant women living near a chemical plant in Tianjin had a risk of exposure to dioxins. Concentrations of PCDD/Fs and dl-PCBs in 24 umbilical cord serum samples collected from pregnant women were measured using a high-resolution gas chromatograph with a high-resolution mass spectrometer (HRGC-HRMS) and an isotopic dilution method. The levels of ∑(PCDD/Fs + dl-PCBs) were in the range 476-8307 pg·g-1 lipid, with a mean of 3037 pg·g-1. The mean World Health Organization toxicity equivalent (WHO-TEQ) for PCDD/Fs and dl-PCBs was 14.0 and 2.14 pg·g-1 lipid, respectively. The PCDD/Fs and dl-PCBs contributed 86.7% and 13.3%, respectively, to the total TEQ. The octa-CDFs and penta-CBs were predominant for the PCDD/Fs and dl-PCBs, accounting for 57.6% and 74.3%, respectively. Several PCDD/F and dl-PCB congeners were highly correlated, such as PCB 105 and PCB 118 (r = 0.982, p < 0.001). Although the results hint at decreasing trends for PCDD/F and dl-PCBs by comparison with a similar study in Tianjin, a total TEQ of 41.7% of study participants had a body burden that exceeded the biomonitoring equivalents for dioxins. It was shown that pregnant women and infants had a health risk of exposure to dioxins.

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Benzo [a]pyrene (BaP) is a model compound for the study of polycyclic aromatic hydrocarbon (PAH) carcinogenesis. Upon metabolism, BaP is metabolized to the ultimate metabolite, BaP trans-7,8-diol-anti-9,10-epoxide (BPDE), that reacts with cellular DNA to form BPDE-dG adducts responsible for BaP-induced mutagenicity, carcinogenicity, and teratogenicity. In this study, we employed our developed LC-MS/MS method to detect and quantity BPDE-dG adducts present in 42 normal human umbilical cord blood samples and 42 birth defect cases. We determined that there is no significant difference in the level of BPDE-dG formation between the normal and birth defect groups. This represents the first time to use an LC-MS/MS method to quantify BPDE-dG in human umbilical blood samples. The results indicated that under experimental conditions, BPDE-dG adducts were detected in all the human umbilical cord blood samples from the normal and birth defect groups.

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Background: Exposure to heavy metals during pregnancy is an important risk factor for adverse birth outcomes. We aimed to investigate the current heavy metal exposure levels in cord blood from healthy pregnant women residing in the Huaihe River Basin, China, and examined the association between heavy metal levels and dietary habits and lifestyle factors. In this study, we measured the exposure levels of five heavy metals in the umbilical cord blood from 350 healthy pregnant women and administered 350 self-reported questionnaires regarding the general characteristics and dietary habits of those women. Methods: This study was undertaken in Shenqiu county, Henan province, which is in the area of the Huai River Basin, in a cohort of pregnant women and newborn babies in 2013-2014. We recruited a sample of 1000 pregnant women among those receiving prenatal examination, measured the real individual newborn exposure to heavy metals in serum by ICP-MS, collected information regarding the pregnant women with a questionnaire survey and obtained data on environmental quality from environmental protection agencies and the available literature. We estimated the daily individual exposure to heavy metals of all the 1000 participants throughout the pregnancy and recorded their birth outcomes after delivery. Then we analyzed the association between birth outcome and individual exposure to heavy metals. Results: 54 newborn children had birth defects. The geometric means of cord blood levels of As, Cd, Cr, Pb and Hg were measured at 0.92 ± 1.01 ng mL-1, 0.11 ± 0.17 ng mL-1, 4.57 ± 5.02 ng mL-1, 3.37 ± 3.81 ng mL-1 and 0.89 ± 1.69 ng mL-1 for subjects (n = 54) who gave birth to infants with birth defects and 0.43 ± 0.88 ng mL-1, 0.52 ± 3.86 ng mL-1, 1.94 ± 2.92 ng mL-1, 4.38 ± 4.96 ng mL-1 and 0.43 ± 0.91 ng mL-1 for subjects (n = 296) with healthy infants, respectively. The contents of all five heavy metals in the whole blood of both of these two groups were higher than the reference values of the Chinese general population (P < 0.001). Conclusions: The occurrence of birth defects was 15.4% in this cohort, and was correlated to exposure of parents to environments containing heavy metal contaminants in Shenqiu county in the Huai River Basin. The heavy metal exposure situation of the investigated population had serious effects in terms of reproductive defects in children. The specific link between newborn defects and environmental heavy metal contaminants suggested that contamination in pregnant women persisted over time, and that the exposure may have a long term effect.

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Although animal studies have found that perfluoroalkyl substances (PFASs) affect gestational and postnatal growth, the epidemiological findings are limited and not in agreement. We explored the associations of PFAS concentrations in umbilical cord blood with gestational and postnatal growth in China. Three hundred thirty-seven singleton newborns and their mothers were recruited from November 2013 to December 2015 in Zhoukou City, China. Umbilical cord blood was collected to measure eleven PFASs by liquid chromatography-mass spectrometry. The index of gestational and postnatal growth contained fetal weight, length, and head circumference. These were obtained at birth and at the follow-up investigation (mean 19 months). Exposed to higher perfluorooctanoic acid (PFOA) were connected with reduced length at birth (p for trend = 0.01) and decreased postnatal weight (ß = -429.2 g; 95% CI: -858.4, -0.121 for 2nd VS. 1st). Exposed to perfluoroundecanoic acid (PFUdA) were positively associated with indications of gestational growth and postnatal growth (p for trend = 0.02 for birth length; p for trend = 0.04 for postnatal length). Exposed to higher perfluorododecanoic acid (PFDoA) were associated with lower birth weight (ß = -122.9 g, 95% CI: -244.7 to -1.2 for 2nd VS. 1st), but higher postnatal length (p for trend = 0.03). Neonates in the highest exposure group of per-fluorohexanesulfonate (PFHxS) showed decreased birth length (ß = -0.33 cm, 95% CI: -0.68 to -0.01, for 2nd VS. 1st), but increased postnatal head circumference (p for trend = 0.04). Increased PFOA concentrations was associated with shorter birth length only in girls (p for trend = 0.04), suggesting that the effect of PFASs on gestational growth were different between boys and girls. In utero exposure to PFASs may affect gestational and postnatal growth.

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Organochlorine pesticides (OCPs) had been widely used in agriculture and disease prevention from the 1940s-1960s. Currently, OCPs are raising global concerns due to their associated prevalent contamination and adverse health effects, such as endocrine disruption. Several epidemiological studies have explored the underlying association of OCPs on thyroid hormone (TH) status in adults and newborns, but the results of studies performed on newborns are often inconclusive. This exploratory study was conducted with the purpose of assessing the potential association of the prenatal exposure to OCPs with the concentrations of TH in the cord blood of newborns from China. Cord blood and information on demographic characteristics were collected from 115 newborns between November 2013 and June 2014. The exposure levels of 17 OCPs were measured with a gas chromatography/mass spectrometry, and TH levels including free triiodothyronine (FT3), free thyroxine (FT4), and thyroid-stimulating hormone (TSH) were detected using electrochemiluminescence immunoassay methods. After adjusting for confounding factors (the age of pregnant mothers, education level, monthly household income, parity, and sex of the newborns), we found marginally significant inverse associations of cord plasma measurements of ∑hexachlorcyclohexanes (∑HCHs), 1,1-dichloro-2,2-di(4-chlorophenyl)ethylene (ρ,ρ'-DDE) and methoxychlor with FT4 levels, but not with FT3 and TSH levels. Moreover, higher cord plasma levels of aldrin, dieldrin, ∑dichlorodiphenyltrichloroethanes (∑DDTs), ∑Drins, and ∑OCPs were found to be related to the increase in cord plasma TSH levels after the adjustment for confounders. The results of this exploratory study indicate that in utero exposure to certain OCPs may affect TH status in newborns, and therefore, pose potential effects on early human development. Further research, with larger sample sizes, should be conducted to confirm these findings.

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Organochlorine pesticides (OCPs), one of the persistent organic pollutants (POPs) with highly lipophilic properties, long half-lives, and persistence in the environment, are prevalent in the environment even though they have been banned for >30years. We aimed to investigate the current OCP exposure levels in cord blood from healthy pregnant women residing in the Huaihe River Basin, China, and examined the association between OCP levels and dietary habits and lifestyle factors. In this study, we measured the exposure levels of 17 OCPs in the umbilical cord blood from 999 healthy pregnant women; we also administered 1000 self-reported questionnaires regarding the general characteristics and dietary habits of those women. Our results showed that ρ,ρ'-DDE, ρ,ρ'-DDT, aldrin, dieldrin, and methoxychlor, which had higher measured concentrations (2.01±1.89, 4.31±5.68, 7.29±8.74, 5.27±7.65, and 0.98±1.42ng/mL, respectively) and detection frequencies (99.69%, 100.00%, 81.79%, 75.00%, and 74.49%, respectively), were the predominant OCPs in cord blood, and the higher levels of DDTs, aldrin, dieldrin, and methoxychlor were mainly due to recent use. In addition, most of the HCHs in cord blood were derived not only from historical use of technical HCH, but also from the additional use of lindane. In addition, we found that the education level of the pregnant women and monthly household income were positively correlated with OCP levels, particularly ρ,ρ'-DDE, aldrin, and dieldrin. Furthermore, the consumption of red meat (pork, beef, and lamb), fish, and bean products may be an important contributing factor to the increased concentrations of OCPs in cord blood, while the intake of poultry and pickles was negatively correlated with aldrin level. This study is the first to provide adequate data on current OCP exposure levels in cord blood from pregnant women in the Huaihe River Basin.

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Benzene exposure has been causally linked with acute myeloid leukemia (AML), but inconsistently associated with other hematopoietic, lymphoproliferative and related disorders (HLD) or solid tumors in humans. Many neoplasms have been described in experimental animals exposed to benzene. We used Poisson regression to estimate adjusted relative risks (RR) and the likelihood ratio statistic to derive confidence intervals for cause-specific mortality and HLD incidence in 73,789 benzene-exposed compared with 34,504 unexposed workers in a retrospective cohort study in 12 cities in China. Follow-up and outcome assessment was based on factory, medical and other records. Benzene-exposed workers experienced increased risks for all-cause mortality (RR = 1.1, 95% CI = 1.1, 1.2) due to excesses of all neoplasms (RR = 1.3, 95% CI = 1.2, 1.4), respiratory diseases (RR = 1.7, 95% CI = 1.2, 2.3) and diseases of blood forming organs (RR = ∞, 95% CI = 3.4, ∞). Lung cancer mortality was significantly elevated (RR = 1.5, 95% CI = 1.2, 1.9) with similar RRs for males and females, based on three-fold more cases than in our previous follow-up. Significantly elevated incidence of all myeloid disorders reflected excesses of myelodysplastic syndrome/acute myeloid leukemia (RR = 2.7, 95% CI = 1.2, 6.6) and chronic myeloid leukemia (RR = 2.5, 95% CI = 0.8, 11), and increases of all lymphoid disorders included excesses of non-Hodgkin lymphoma (RR = 3.9, 95%CI = 1.5, 13) and all lymphoid leukemia (RR = 5.4, 95%CI = 1.0, 99). The 28-year follow-up of Chinese benzene-exposed workers demonstrated increased risks of a broad range of myeloid and lymphoid neoplasms, lung cancer, and respiratory diseases and suggested possible associations with other malignant and non-malignant disorders.

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OBJECTIVE: To explore the correlation between the expression of tumor suppressor gene p15 and the hematotoxicity from benzene exposure. METHODS: Twenty cases of patients with chronic benzene poisoning (BP), 17 benzene-exposed workers engaged in the same job with the patients but without BP and 19 matched unexposed controls from Tianjin were recruited. The expression of tumor suppressor gene p15 mRNA was detected by qRT-PCR. RESULTS: Comparing with the unexposed controls, the expression levels of p15 mRNA were significantly down-regulated in BP patients (P < 0.01) and also in benzene-exposed workers (P < 0.01). The expression of p15 was down-regulated with the increased severity of BP (P < 0.01). The expression of p15 mRNA is positively correlated with white blood cell counts and neutrophil counts (r = 0.42, P = 0.002, r = 0.44, P = 0.002, respectively). CONCLUSION: The expression of p15 mRNA is significantly down-regulated in BP patients. The transcriptional repression of p15 is associated with benzene hematotoxicity.

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OBJECTIVE: To investigate whether benzene negatively affects the expression of p16 through DNA methylation. METHODS: We carried out a case-control study in Chinese occupational benzene poisoning patients. Eleven cases of BP and 8 controls who were matched for age (+/- 5 years), sex, working duration and job title with BP were recruited. Expression level was examined by quantitative real-time PCR. Bisulfite-PCR pyrosequencing was used to quantitate the level of DNA methylation. RESULTS: The expression levels of p16 are down-regulated in BP patients compared to the control group (0.53 versus 2.06, P = 0.064). The average percentage of methylated cytosines of p16 was higher in BP group than in controls (12.4%, 11.3%, respectively, P > 0.05). p16 mRNA level decreased with increasing methylation (Pearson r = -0.64, P > 0.05). The fourth CpG site in p16 promoter is located within the consensus binding sequence for olfactory neuron-specific transcription factor. A significant negative correlation between mRNA level and the fourth CpG site was exhibited (Pearson r = - 0.88, P < 0.05). CONCLUSION: Our report demonstrated that mRNA expression of p16 is significantly downregulated in BP patients. Hypermethylation in promoter CpG islands is likely to contribute to the downregulation of p16. Further in-depth studies, utilizing large number of samples, are needed to fully understand the molecular mechanism involved in the tumor-suppressor gene inactivation in benzene-related diseases.

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